43-year-old man infected with HCV genotype 1a and human immunodeficiency virus (HIV), with liver fibrosis grade F4 (cirrhosis), FibroScan of 27 kPa and Child-Pugh grade A. On HIV treatment since February 2010 (tenofovir + emtricitabine + raltegravir).
The patient presented RP below normal levels (<120 x 109/L) since diagnosis of HCC (December 2008). Prior to initiation of antiviral therapy for HCC, the patient had grade III thrombocytopenia (PR = 42 x 109/L), grade III neutropenia (neutrophils = 0.66 x 109/L) and haemoglobin (Hb) values within normal range (Hb = 14.1 g/dL). Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) values were within normal range (35 and 36 IU/mL, respectively) and gamma-glutamyltranspeptidase (GGT) was found slightly elevated (62 IU/mL). HCV viral load (CVVHC) was 180,000 copies/mL and CVHIV was undetectable.
In March 2012 he started treatment for HCC with pegIFN-α2a and RBV (180 mcg/week and 1,000 mg/day, respectively) for 11 weeks. At week 12, presenting with a PR of 26 x 109/L, TVR (750 mg/8hours) was added. The PR decreased progressively to 16 x 109/L at week 14, at which time treatment with eltrombopag 50 mg/day was started and the dose of pegIFN-α2a was reduced to 135 mcg/week. At weeks 16 and 17 the PR remained below normal values (14 x 109/L and 13 x 109/L, respectively). At week 22 the PR rose to 34 x 109/L and the dose of eltrombopag was increased to 75 mg/day, the type of IFN (from pegIFN-α2a to pegIFN-α2b) and its dose (from 135 mcg to 80 mcg/week) was changed to coincide with the end of TVR treatment. The dose of eltrombopag was reduced to 50 mg/day at week 30 and at week 35 it was discontinued due to a PR of 50 x 109/L. At the end of treatment (week 48), the PR was 67 x 109 platelets/L with undetectable CVVHC (< 15 copies/mL) since week 15.